In cases of occupational lung diseases like silicosis, it is important to note the duration of exposure, the type of work which helps us to understand the type of silica to which they are exposed, history of use of any protective devices, etc. Also, obtain information about similar affections among other people around.
Silicosis is divided into 3 different types depending on the duration of its occurrence :
Simple chronic silicosis occurs after long term exposure (20 years or more) to small amounts of silica dust. This is the commonest form of silicosis. The chronic silica exposure leads to swelling of the lung and lymphatic tissue. The patient remains asymptomatic for years or may experience exertional dyspnea and cough with sputum. History of smoking or bronchitis may worsen the symptoms or hasten their pace. On physical examination, the lungs appear normal, but in some cases rhonchi or rhales may be audible on auscultation.
Accelerated silicosis occurs after exposure for 5 to 15 years to larger amounts of silica dust. Swelling in the lungs and symptoms occur faster than in simple silicosis. The symptoms are similar to simple chronic silicosis, but they manifest in a shorter duration.
Acute silicosis occurs after a short-term i.e. around 1 year exposure to very large amounts of silica dust. In such cases, the lungs are inflamed and may also have fluid accumulations. This leads to low oxygen levels and dyspnea. There may be pleuritic pain accompanying the other symptoms. Over months, patients may complain of weight loss and exhaustion. On examination, one may hear diffuse bilateral crackles. In some cases, respiratory failure may occur over a period of 2 years.
Progressive massive fibrosis or conglomerate or complicated silicosis produce even more severe respiratory symptoms. There is severe lung scarring and destruction of the normal lung tissue. This presents with severe dyspnea even at rest, productive cough, severe fatigue and weight loss. On examination the findings may include tachypnea, expiratory prolongation, rhonchi, wheezing and rhales. Cyanosis may be seen in some advanced cases.
In silicosis, the breath sounds diminish gradually, duration depending on the type of silicosis. It leads to pulmonary consolidation and pulmonary hypertension . Finally, respiratory failure with or without right ventricular failure may ensue in advanced pathological cases of silicosis. In patients suffering from silicosis the chances of developing pulmonary tuberculosis are about 2.8 to 39 times higher as compared to healthy individuals .
Any patient suspected of silicosis must be questioned in detail about their occupation, years of exposure, work performed and materials used. Physical examination findings must also be noted. This history helps us in diagnosing the disease and knowing its intensity and prognosis.
Imaging techniques performed to detect Silicosis include chest X-ray and CT scan of the chest. A CT scan is more sensitive and confirmatory as compared to an X-ray. X-rays are efficient at detecting most diseases, but a CT shows well-defined lung architecture and pathology .
The Internation Labour Organisation has developed a classification called as International Classification of Radiogrphs of Pneumoconiosis. This scale is standardized and mentions the size and shape of opacities, their concentrations and the accompanying pleural changes visible on the X-ray.
In acute silicosis, chest X-ray shows diffuse alveolar bibasilar opacities due to the fluid filled alveoli. Chest CT shows bilateral centrilobular and mutlifocal consolidation or ground-glass opacities . In chronic silicosis 1 to 10 mm round opacities or nodules are seen on chest X-ray or chest CT, more commonly in upper lung fields. Calcification of these nodules may also be visible in some cases . Calcified hilar and mediastinal lymph nodes which look like egg shells are detected in most cases of silicosis .
Progressive massive fibrosis on X-ray shows bilateral upper lobe masses formed by coalescence of the nodules. Due to fibrosis, these masses are pulled towards the hilum causing the lower lobes to look increased in size. Hilar calcification may also be seen. Bullae may be seen around the conglomerate masses. Large masses which compensate the volume of the lungs can lead to tracheal deviation. In cases who suffer from rheumatoid arthritis (RA) as a complication of silicosis, 3 to 5 mm pulmonary rheumatoid nodules are visible on chest X-ray or chest CT.
Pulmonary function tests
In simple silicosis, the results may show mildly reduced lung volume with normal functional residual capacity and residual volume. In advanced cases of silicosis, there is airflow obstruction restricting the airways, decreased lung volumes, decreased diffusing capacity for carbon monoxide. Arterial blood gases show hypoxemia.
Tuberculin skin test
A tuberculin skin test using purified protein derivative (PPD) must be performed in cases suffering from silicosis since they are highly susceptible. Cases which show the test positive i.e. 10 mm or more of induration, must be treated. Also, their sputum must be tested for acid-fast bacilli by microscopy and a culture must be performed.
Diagnosis of silicosis is usually made by the history and imaging studies. Hence, bronchoscopy is not often indicated. It may be performed in cases who show a cavity or a mass lesion and pulmonary tuberculosis or cancer is suspected (especially when sputum test is non-conclusive).
Blood test must be performed to rule out other connective tissue diseases co-existing with silicosis like systemic sclerosis, RA etc. These may show presence of anti-nuclear antibodies (ANA) and elevated rheumatoid factor.
To ensure effective treatment of silicosis, it is important to remove the source of silica exposure to prevent worsening of the disease. In some cases of silicosis, a whole lung lavage is used. It helps to decrease the dust load in the lungs. Research shows that a lavage helps to relieve the symptoms for a short duration.
Though it is not proven, oral corticosteroids are known to be more effective in acute silicosis rather than chronic silicosis. Patients who smoke must be advised to stop smoking and must be helped to quit the habit. Practical experiences have shown that bronchodilators and inhaled corticosteroids alleviate the symptoms of airway obstruction in cases of silicosis.
Cases of silicosis along with latent tuberculosis must be treated with isoniazid for 9 months twice weekly as suggested by the treating physician under strict supervision. While active cases of tuberculosis must be treated aggressively with combinations of isoniazid, rifampin, pyrazinamide, streptomycin and ethambutol. The dosages should be as per the guidelines for treating tuberculosis. Studies have proven that a 4-month rifampcin course is more advisable as compared to a 9-month isoniazid course as it has higher patient compliance and lower adverse reactions and toxicity .
Complications like pulmonary hypertension, cor pulmonale or respiratory failure must be treated according to the standard treatment. Pulmonary rehabilitation helps the patient to improve lung function and perform daily activities. A study done in the University Hospital of Munich showed pulmonary rehabilitation for 12 months helped reduce the rate of exacerbations by 35%, antibiotic therapy by 27% and use of health care services by 17% . With present advances in medicine, lung transplantation is a possible alternative in cases with end-stage silicosis as it can greatly improve quality of life and survival .
The clinical presentation at the time of diagnosis is somewhat predictive of the prognosis, but the rate of progression varies. Silicoproteinosis worsens quickly, and death may occur in months. Progressive massive fibrosis causes gradual worsening of symptoms, deterioration of lung function, and increasing disability. On the other hand, patients with simple silicosis may be asymptomatic and may remain stable for many years, both clinically and radiographically. Simple chronic silicosis remains asymptomatic for years and hence, the patients remain stable. Acute silicosis manifests severe symptoms quickly and therefor, affects the lung functioning at a faster pace disabling the patient.
Conglomerate or complicated silicosis also known as progressive massive fibrosis, is a more severe form and leads to extensive lung damage and fibrosis; severely compensating the lung functions. This renders the patient completely disable due to irreversible pulmonary damage. Eventually, cor pulmonale and respiratory failure ensue.
Since the lung functioning is affected, complications cause related morbidity. Also, there is an increased chance of other lung disorders like pneumothorax, broncholithiasis, brochial obstructions, emphysema etc.
Silica is an important constituent of the Earth’s crust. Silica is found in non-crystalline and crystalline forms. The crystalline forms are deemed to be pathogenic. Quartz is the commonest form of silica. Inhalation of the tiny dust particles of crystalline silica and their deposition in the lungs causes the disease silicosis. Workers in occupations like mining, quarrying, drilling, crushing stone, chipping, sandblasting, pottery or stone work, blast furnaces, coal mining and glass manufacturing are constantly exposed to these particles and are at a high risk of developing silicosis.
Usually, it takes constant exposure of nearly 15 to 20 years before one experiences the symptoms of silicosis. Intense constant exposure to silica at times can manifest the disease in a year. The development of silicosis depends on the duration and intensity of the exposure to silica particles. The crystalline form of silica dust poses a higher risk than its other forms. When these particles are inhaled immediately after being released, they tend to be even more harmful.
Silicosis is said to be the commonest occupational lung disease all over the world. It occurs everywhere, but it is more frequent in developing countries. In USA, it is estimated that only one-third of the total cases of silicosis are reported. It is impossible to assess accurately the frequency of the disease due to various issues like improper records and delayed diagnosis and treatment. In USA, the number of deaths from silicosis declined from 1,065 in 1968 to 165 in 2004 .
In India, there are over 3 million workers exposed to silica dust, while 8.5 million are exposed to quartz. Silicosis is common all over India, especially in the central and western India. It is one of the important causes of morbidity .
When the free silica particles are inhaled they enter the respiratory tract. There they are ingested by alveolar macrophages which then enter the lymphatic and interstitial tissues. This results in release of cytokines i.e. tumour necrosis factor- α, interleukin-1, growth factors i.e. tumour growth factor β and other chemotactic factors. These stimulate parenchymal inflammation damaging the resident cells and the extracellular matrix. The fibroblasts proliferate and collagen is synthesized. The final stage of this is fibrosis of the lung tissue.
After the death of the macrophages, the silica particles are again released into the respiratory tract forming silicotic nodules. Macrophages, lymphocytes, fibroblasts and collagen particles are enclosed in these nodules. On maturation, fibrotic scarring occurs within the nodules which are surrounded by inflammatory cells.
In cases of low-intensity or short-term exposure, the nodules continue to be asymptomatic and do not affect the lung functioning. In cases of high-intensity or long-term exposures, the nodules combine together and lead to fibrosis which accelerates over time. This reduces the lung capacity and functioning. In certain cases, these nodules combine to form large conglomerate masses known as progressive massive fibrosis.
The Occupational Safety and Health Administration (OSHA) has set a permissible exposure limit for respirable silica of 10 mg/m3. The National Institute for Occupational Safety and Health (NIOSH) standard is a more stringent exposure limit of 0.05 mg/m3. By law, it is the responsibility of the employers to take the correct measures to protect the health of their employees.
Silicosis is a totally preventable disease. The employer must provide the correct equipment and clothes that are needed to protect against inhaling silica dust. It is the duty of the employee to use these protective wear and protect themselves. Use of commercially available shrouds when grinding sandstone with a 5-inch angle grinder in restoration stonework can reduce respirable silica dust by 90-99% .
To prevent exposure to silica or keep it to the minimum possible one must follow the below mentioned precautions at the workplace:
The National Institute of Occupational Safety and Health approves specific respirators for specific situations. The type of respirator needed depends on two things. One the amount of silica dust exposed and two the kind of work involved.
Along with these precautions at the workplace, one must maintain personal hygiene to prevent development of silicosis:
Silicosis is a lung disease, a type of pneumoconiosis. It is an occupational hazard as it is most commonly found in miners, sand-blasters and glass workers. It is an incapacitating, irreversible and sometimes incurable lung disease which occurs following inhalation of dust that contains crystalline silicon dioxide i.e. silica or its other forms . Granite, slate and sandstone contain abundant free silica. Overexposure to silica particles causes inflammation and scarring of the lung tissue along with nodular lesions . Hence, it is a fibronodular lung disease. In 1870, Visconti was the first to use the name silicosis .
Silicosis was also known as miner’s phthisis, grinder’s asthma or potter’s rot. In 1935, another name for silicosis was invented by Everett M. Smith, which is the largest 45 letter English word – pneumonoultramicroscopicsilicovolcanoconiosis .
Silicosis is an occupation-related lung disease. It is commonly seen among workers working in occupations like mining, quarrying, drilling, crushing stone, chipping, sandblasting, pottery or stone work, blast furnaces, coal mining, glass manufacturing etc.
Silicosis can be simple, chronic which occurs in workers exposed to small amounts of silica dust for over 20 years. One can have accelerated silicosis, which occurs after being exposed to larger amounts of silica for 5 to 15 years. It can also be a diagnosis of acute silicosis in workers exposed to very large amounts of silica for a year. The most severe form of silicosis is called progressive massive fibrosis or complicated silicosis.
The symptoms of silicosis depend on the intensity and type of silicosis. They include shortness of breath on exertion initially and then even on rest, cough with sputum and in advanced stages is accompanied with weight loss and fatigue.
On auscultation, there is are sounds like ronchi, rhales, wheezing etc. depending on the type of silicosis. Silicosis can be diagnosed on chest X-ray or chest CT scan. Pulmonary function tests show the compensation of the lungs due to silicosis. A tuberculin skin test is a must to rule out secondary tuberculosis in these patients. Other blood tests are performed to check other connective tissue diseases.
Treatment of silicosis includes lung lavage, corticosteroids and bronchodilators. Anti-tubercular drugs are used to treat tuberculosis. Other complications are treated with their specific treatments. Silicosis is a preventable disease. Workers must use specific clothes, respirators etc. to keep themselves from inhaling the silica dust. They must maintain a good personal hygiene so that they do not carry home the silica dust.